Risk estimates, extrapolated from studies of underground miners, predict that residential radon progeny exposure accounts for approximately 19,000 lung cancer deaths each year in the United States. Previous case-control epidemiologic studies, which examined the relationship between residential radon exposure and lung cancer, lacked the ability to verify these risk estimates. Inaccurate dose assessment of radon exposure, a high percentage of proxy respondents, inadequate pathologic review, and low residential radon concentrations led to exposure misclassification and limited the interpretation of these studies. The Iowa Radon Lung Cancer Phase I study was designed to overcome many of these limitations. The Phase I study utilized advanced radon dose assessments, independent histologic review, and a study population that was characterized by geographic stability, high percentage of live cases, and potential for high radon exposure. The Phase I study demonstrated that exposure to residential radon gas increases the risk of developing lung cancer. To refine these estimates, we now propose Phase II studies that examine the association between residential radon product (progeny) exposure and the development of lung cancer. Because radon progeny deliver the actual radiation dose to the lung tissues, rather than radon gas itself, in order to reduce further the exposure misclassification, radon dose estimates need to take into account exposure to residential radon progeny. This requires measuring actual airborne radon progeny concentrations and integrating the exposure to radon progeny over time. The Phase II study will derive more accurate retrospective radon dose estimates by using a novel retrospective radon progeny integrating glass-based detector. Specific Aim I examines the hypothesis that exposure to residential radon progeny is associated with increased risk of developing lung cancer, after controlling for confounders. We will perform field calibration and laboratory validation of the retrospective radon "glass" detectors, and analyze the risk estimates by incorporating exposures to radon progeny, rather than exposures to radon gas. Specific Aim II will determine whether the shape of the dose response curve that best describes the relationship between residential radon progeny exposure and lung cancer risk is linear or nonlinear. Specific Aim III will examine whether exposure to radon progeny contributes to the development of adenocarcinoma, as well as other lung cancer histologic types. For Aims II and III we will use pooled analyses of exposure estimates that are derived from retrospective radon progeny "glass" detectors for subjects from the Iowa and Missouri Radon Lung Cancer Studies. The pooling of data between two large-scale epidemiologic studies from a similar geographic area, Iowa and Missouri, will allow us to increase sample size and statistical power.